In the mammalian embryonic trunk, neural crest cells emigrate from the
closed neural tube in a cranio-caudal sequence and appear to have sim
ilar migration pathways and derivatives to those of avian embryos. In
the cranial region, however, there are mammalian-specific features, wh
ich are related to the mammalian-specific pattern of cranial neurulati
on. Midbrain and rostral hindbrain neural crest cells emigrate from wi
dely open neural folds; caudal hindbrain crest emigrates in a caudo-ro
stral sequence, following the sequence of neural tube closure in this
region. The forebrain is also a source of neural crest cells at early
stages of neurulation; both forebrain and midbrain crest cells contrib
ute to the frontonasal mesenchyme, although their relative contributio
ns have not been analysed. Few studies have provided direct informatio
n about mammalian neural crest cell derivatives. Studies on the effect
s of retinoid excess on craniofacial development provide indirect evid
ence that mammalian cranial neural crest, like that of avian embryos,
includes two populations whose differentiated phenotype and morphologi
cal tissue structure are determined prior to emigration. Retinoid-indu
ced shortening of the preotic hindbrain leads to abnormal migration pa
thways of the neural crest cells that normally migrate into the mandib
ular arch to form Meckel's cartilage, so that an ectopic Meckel's cart
ilage-like structure forms in the maxillary region of the face. Slow d
escent of the heart in retinoid-exposed embryos enables the ''wrong''
crest cell population to populate the wall of the truncus arteriosus.
These observations correlate well with observations of retinoid-induce
d craniofacial and heart abnormalities in human infants.